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520 W. J. Ott<br />

Table 35.1. Causes of heart failure: comparison of adult<br />

and fetal causes<br />

Cause Adult Fetus<br />

Cardiac arrhythmia Disorders of<br />

arrhythmia<br />

Decreased<br />

contractility<br />

Metabolic<br />

disorders<br />

Anoxia/ischemia<br />

Myocarditis<br />

Cardiac anomalies Congenital or<br />

acquired<br />

Increased peripheral<br />

demand<br />

Increased<br />

afterload<br />

Increased preload<br />

Decreased venous<br />

return<br />

Myocarditis<br />

Systemic infection<br />

Anemia<br />

AVshunts<br />

Hypertension<br />

Valvular stenosis<br />

Valvular<br />

regurgitation<br />

Hemorrhage<br />

Vena cava obstruction<br />

Congenital<br />

arrhythmias<br />

Maternal collagen<br />

vascular disease<br />

Maternal<br />

ketoacidosis<br />

Intrauterine<br />

growth restriction<br />

Myocarditis<br />

Congenital<br />

anomalies<br />

Myocarditis<br />

Chorioamnionitis<br />

Systemic infection<br />

Anemia<br />

Fetal tumors<br />

Chorioangioma<br />

Uteroplacental<br />

insufficiency?<br />

Congenital heart<br />

disease<br />

Recipient twin<br />

Indomethacin?<br />

Hemorrhage<br />

(abruption, vasa<br />

previa, fetomaternal,<br />

other)<br />

Venous obstruction<br />

(tumor,<br />

hydrops, other)<br />

Iatrogenic Drug effects Indomethacin,<br />

tocolytics, others<br />

eral venous pressure and fetal decompensation and<br />

cardiac failure. Table 35.1 compares the causes of cardiac<br />

failure in the adult with known or postulated<br />

causes in the fetus.<br />

The Scope of Fetal Cardiac Failure<br />

Changes in obstetrical management, the development<br />

of new and more accurate methods of fetal surveillance,<br />

and a better understanding of the pathogenesis<br />

of fetal demise has led to changes in the distribution<br />

of the causes of stillbirths. Table 35.2 shows the distribution<br />

of stillbirths from a review at the author's<br />

institution for the years 1988 through 1992. There<br />

were four fetal deaths directly caused by fetal heart<br />

failure: one premature closure of the foramen ovale;<br />

one case of non-immune hydrops caused by tachyarrhythmia;<br />

one case of significant increase in cardiac<br />

afterload caused by prune-belly syndrome; and one<br />

case of myocardial hypertrophy with heart failure in<br />

Table 35.2. Causes of fetal death: SJMMC Stillbirths 1988±<br />

1992<br />

Category Number Percentage (%)<br />

Placental<br />

Abruption 13 9<br />

Other 27 a 17<br />

Infection 32 b 21<br />

Anomalies 19 13<br />

Twin complications<br />

Mono/Mono 3 c 2<br />

Twin±twin transfusion 10 d 6<br />

Unknown 2 1<br />

Cord accident<br />

Nuchal 7 5<br />

True knot 2 1<br />

Vasa previa 1 1<br />

Fetal heart failure 4 3<br />

Maternal<br />

Liver rupture 2 1<br />

Ketoacidosis 1 1<br />

Aortic aneurysm 1 1<br />

Unknown 27 18<br />

Fetal trauma: ± ±<br />

Rh: ± ±<br />

Total 151 100<br />

a Includes two sets of twins with three stillbirths.<br />

b Includes one set of twins with two stillbirths.<br />

c Two sets of twins with one survivor.<br />

d Includes one set of triplets with a single survivor.<br />

a fetus of a diabetic mother. Although only 3% of fetal<br />

deaths were directly caused by fetal heart failure,<br />

it most likely played a significant role in many other<br />

fetal deaths: heart failure was the most likely terminal<br />

event in the cases of intrauterine infection (21%),<br />

twin±twin transfusion (6%), cord accidents (7%), and<br />

acute maternal problems (3%); and may have play a<br />

role in many of the cases of placental failure (17%). It<br />

is, therefore, likely that fetal heart failure plays a significant<br />

role in at least 40%±50% of stillbirths.<br />

Duplex Doppler Evaluation<br />

of the Fetal Cardiovascular System<br />

Evaluation of fetal cardiac status includes measurements<br />

of velocity parameters in both peripheral vessels<br />

and the heart itself. In peripheral vessels angleindependent<br />

indices, such as the pulsatility index, resistance<br />

index, and systolic/diastolic (S/D) ratio, are<br />

most commonly used. The peripheral vessel most<br />

commonly evaluated is the umbilical artery. Changes<br />

in the velocity indices in this vessel reflect alterations<br />

in placental perfusion that may precede evidence of<br />

heart failure in situations of uteroplacental insufficiency.<br />

Additional peripheral fetal vessels, such as the<br />

aorta, renal arteries, and carotid and middle cerebral

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